摘要
目的:探讨健脑益智口服液在反复脑缺血再灌注损伤中的神经保护机制。方法:实验分为空白对照组、假手术组、模型组、中药组。实验期间空白对照组、假手术组、模型组以蒸馏水灌胃,中药组以健脑益智口服液灌胃,用药5d后实施脑缺血再灌注术。手术后第1,10天,小鼠断头取脑以测定超氧化物歧化酶(SOD)的活性、丙二醛、肿瘤坏死因子α(TNF-α)以及白细胞介素1β(IL-1β)的表达。结果:与对照组(26.82±3.58)mg/g相比,模型组鼠脑缺血再灌注后SOD活性第1天(13.95±4.52)mg/g和第10天(15.82±4.39)mg/g明显降低,丙二醛、TNF-α,IL-1β含量显著升高。与模型组相比,健脑益智口服液能显著提高SOD犤(21.35±4.07)mg/g犦的活性(F=16.56,q=3.29,P<0.05),并降低丙二醛的水平(F=81.88,q=34.61,P<0.01)。健脑益智口服液能显著下调小鼠大脑皮质TNF-α(F=96.44,q=35.11,P<0.01)和IL-1β(F=38.30,q=40.92,P<0.01)的水平。结论:健脑益智口服液通过降低脑缺血再灌注后脑氧化反应以及TNF-α和IL-1β表达而起到神经保护作用。
AIM:To investigate the neuroprotective mechanism of jiannoa yizhi tang in treatment of repetitive cerebral ischemia-reperfusion injury. METHODS:Totally 70 mice were randomly divided into seven groups of 10 mice each:bland control group,sham operative groups of 1 and 10 days, model groups of 1 and 10 days,herb groups of 1 and 10 days(jiannao yizhi tang).The mice in the herb groups were gastroperfused with jiannao yizhi tang,while those in the other group with distilled water, both followed by cerebral ischemia-reperfusion 5 days later.One and ten days after operation, the brains were taken out following rapid decapitation to measure the activity of superoxide dismutase(SOD) and the contents of malondialdehyde(MDA),tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β).RESULTS:The activities of SOD were significantly reduced to(13.95±4.52) mg/g and(15.82±4.39) mg/g respectively at 1 and 10 days after cerebral ischemia-reperfusion,as compared with the control group [(26.82±3.58) mg/g]; While the contents of MDA,TNF-αand IL-1βwere significantly increased. In comparison with the model group,jiannao yizhi tang was effective to increase the activity of SOD[(21.35±4.07) mg/g,F=16.56,q=3.29,P< 0.05] and decrease the contents of MDA(F=81.88,q=34.61,P< 0.01).Jiannao yizhi tang had a down-regulative role in the contents of TNF-αand IL-1β(F=96.44,q=35.11,P< 0.01;F=38.30,q=40.92,P< 0.01). CONCLUSION:Jiannao yizhi tang plays a neuroprotective role in the repetitive ischemia-reperfusion injury through reducing oxidation and down-regulating the expression of TNF-αand IL-1βin the brain.
出处
《中国临床康复》
CAS
CSCD
2004年第7期1306-1307,共2页
Chinese Journal of Clinical Rehabilitation
